A team of researchers has gained new insight into how memories are strengthened. The findings may aid in the development of better treatments for temporal lobe epilepsy. The details are in a paper that was just published in the journal Nature.
When a new memory is formed, the connections between neurons are strengthened. These connections, called synapses, allow neurotransmitters to pass through, enabling communication between neurons. As memories become stronger, the part of the neuron that receives these inputs becomes larger. These are known as dendritic spines and they help store and transmit neural signals. One neuron may contain thousands of spines. Scientists know that the growth of these spines strengthens existing memories but the exact mechanisms behind this growth were unknown.
Researchers from Duke University investigated the brain receptor TrkB, long thought to be involved in dendritic spine growth. The team used a fluorescence resonance energy transfer-based sensor to track TrkB activity in a single mouse neuron. They first confirmed the role of TrkB in spine growth; the receptor was active in the spine when the team stimulated growth. The team then added glutamate, a signal that encourages the growth of dendritic spines. The spines grew when this signal was added, but only if the TrkB receptor was present. The researchers also found that a protein called brain-derived neurotrophic growth factor (BDNF) was released from both the receiving and sending neurons during spine growth. This was a new finding; it was previously believed that BDNF was only produced by the neuron sending the signal.
The team’s findings may lead to a better understanding of temporal lobe epilepsy. This common form of epilepsy is sometimes triggered by seizures in early development. During these events, large amounts of glutamate are released and TrkB receptors become active. By researching these neural mechanisms, we can learn more about memory formation while also developing methods for preventing temporal lobe epilepsy after seizure events.
Harward et al. Autocrine BDNF–TrkB signalling within a single dendritic spine. Nature (2016).